Kang Ok-Hwa, Lee Go-Hoon, Choi Hyuk Joon, Park Pil Sang, Chae Hee-Sung, Jeong Seung-Il, Kim Youn-Chul, Sohn Dong Hwan, Park Hyun, Lee John Hwa, Kwon Dong-Yeul
Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk 570-749, Republic of Korea.
Pharmacol Res. 2007 Apr;55(4):263-70. doi: 10.1016/j.phrs.2006.12.001. Epub 2006 Dec 19.
Angelica dahurica (Umbelliferae) has been used to treat headache of common cold, supraorbital neuralgia, painful swelling on the body, nasal stuffiness, leukorrhea and arthralgia due to wind-dampness in Korean traditional medicine. It is also claimed to be effective in the treatment of acne, erythema, headache, toothache, sinusitis, colds and flu. The present study focused whether the ethyl acetate extract from Angelica Dahuricae Radix (EAAD) inhibits production of nitric oxide (NO), prostaglandin E(2) (PGE(2)) and tumor necrosis factor (TNF)-alpha, as well as expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinases (MAPKs) in lipopolysaccharide (LPS)-stimulated macrophages. EAAD inhibited LPS-induced NO, PGE(2) and TNF-alpha production as well as expression of iNOS and COX-2 in RAW 264.7 cells. EAAD inhibited LPS-induced TNF-alpha production in THP-1 cells. Furthermore, EAAD suppressed LPS-induced phosphorylation of p38 MAPK and extracellular-signal regulated kinases 1/2 (ERK1/2), I-kappaBalpha degradation, and NF-kappaB activation in RAW 264.7 cells. These results suggest that EAAD has the inhibitory effects on LPS-induced TNF-alpha, NO and PGE(2) production, and expression of iNOS and COX-2 in macrophage through blockade in the phosphorylation of MAPKs, following I-kappaBalpha degradation and NF-kappaB activation.
白芷(伞形科)在韩国传统医学中被用于治疗普通感冒引起的头痛、眶上神经痛、身体肿痛、鼻塞、白带以及风湿性关节痛。据称它对治疗痤疮、红斑、头痛、牙痛、鼻窦炎、感冒和流感也有效。本研究聚焦于白芷根乙酸乙酯提取物(EAAD)是否能抑制脂多糖(LPS)刺激的巨噬细胞中一氧化氮(NO)、前列腺素E2(PGE2)和肿瘤坏死因子(TNF)-α的产生,以及诱导型一氧化氮合酶(iNOS)、环氧化酶-2(COX-2)、核因子-κB(NF-κB)和丝裂原活化蛋白激酶(MAPKs)的表达。EAAD抑制了RAW 264.7细胞中LPS诱导的NO、PGE2和TNF-α的产生以及iNOS和COX-2的表达。EAAD抑制了THP-1细胞中LPS诱导的TNF-α的产生。此外,EAAD抑制了RAW 264.7细胞中LPS诱导的p38 MAPK和细胞外信号调节激酶1/2(ERK1/2)的磷酸化、I-κBα的降解以及NF-κB的活化。这些结果表明,EAAD通过阻断I-κBα降解和NF-κB活化后MAPKs的磷酸化,对LPS诱导的巨噬细胞中TNF-α、NO和PGE2的产生以及iNOS和COX-2的表达具有抑制作用。